This is in contrast to the observation that mouse Ddx3y is able to compensate for the loss of Ddx3x during neural development, insulating male mice from ataxia and seizure phenotypes upon ablation of Ddx3x, but is unable to reverse the susceptibility to hindbrain malignancies conferred by Ddx3x loss (Patmore et al. 2020). The gene discussed is DDX3X; the disease is cerebellar ataxia.